Destructive developmental retinopathies can be induced by infecting neonatal rodents with lymphocytic choriomeningitis virus. Acute lesions, involving all retinal layers, are produced by a cell-mediated immune response to the spread of viral antigen. This fact is attested by the sparing effects of thymectomy or antilymphocyte serum. The latter treatment, however, fails in the long run to prevent blindness, which results in this case from a delayed but progressive degeneration of the photo receptors. This second condition mimics, at the optical microscopical level, the pathology of human retinitis pigmentosa. Both models provide an excellent opportunity to study the role of the immune reaction as a cause of retinal derangement, and to analyze in detail the underlying cytopathogenetic mechanisms. To achieve these goals we propose to apply advanced histopathological an ultrastructural techniques including, among others, immunocytochemical and freeze-fracture methods. In addition, animals affected with a well defined genetic retinal degeneration (RCS) will be studied simultaneously for comparative purposes. The pathogenetic mechanisms operating in these animal models may parallel those responsible for some human developmental retinopathies.